The CCPG1 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for investigating the roles of CCPG1 in autophagy and ER-phagy. This product consists of a heterogeneous pool of MES-OV cells carrying targeted disruptions in the CCPG1 gene, achieved through non-homologous end joining following Cas9-induced double-strand breaks. The polyclonal format preserves the diversity of editing outcomes, providing a robust loss-of-function model for studying CCPG1-dependent processes without clonal selection artifacts. Researchers can use these cells to interrogate the molecular mechanisms by which CCPG1 functions as an ER-phagy receptor, linking ER stress responses to autophagic degradation pathways.
The host cell line, MES-OV, is an epithelial cancer cell line derived from a patient with ovarian clear cell carcinoma. This cell type is widely employed in ovarian cancer research due to its relevance to chemoresistance and aggressive tumor behavior. Clear cell carcinoma exhibits distinct metabolic and stress-response features, making the MES-OV background particularly suitable for examining how autophagy and ER turnover contribute to cancer cell survival. The cells retain key characteristics of the tumor of origin, including epithelial morphology and dysregulated signaling networks, providing a clinically relevant platform for functional studies.
CCPG1 functions as a selective cargo receptor for ER-phagy, a process that degrades portions of the endoplasmic reticulum via autophagy. It directly interacts with ATG8-family proteins??including MAP1LC3A (LC3), GABARAP, and GABARAPL1??through its LC3-interacting region (LIR) motif, tethering ER fragments to nascent autophagosomes. This activity is upregulated by upstream signals such as starvation, ER stress, TFEB activation, and mTORC1 inhibition. Downstream, CCPG1 engagement promotes LC3 lipidation, GABARAP recruitment, and formation of ER-containing autophagosomes, which ultimately fuse with lysosomes mediated by LAMP2. The pathway integrates inputs from the ULK1 initiation complex, ATG13, Beclin1, and the ATG5-ATG7 conjugation system, positioning CCPG1 as a critical node linking nutrient-sensing and organelle homeostasis.
In the MES-OV ovarian cancer context, disruption of CCPG1-mediated ER-phagy has profound implications for understanding tumor cell resilience. Ovarian clear cell carcinoma cells often face heightened ER stress due to secretory demands, hypoxia, and chemotherapeutic challenge, and they rely on autophagy for survival. Loss of CCPG1 is expected to impair selective ER degradation, leading to accumulation of misfolded proteins, amplified unfolded protein response, and increased sensitivity to ER-stress-inducing agents such as proteasome inhibitors. Consequently, this knockout model enables dissection of how autophagy-dependent mechanisms sustain ovarian cancer progression and may unveil synthetic lethal interactions exploitable for therapeutic intervention.
This polyclonal knockout cell product is ideally suited for a broad range of applications, including mechanistic studies of ATG8-family dependent autophagic pathways, quantitative analysis of ER turnover using autophagy flux assays with bafilomycin A1, and co-immunoprecipitation experiments probing CCPG1 interactions with LC3 or GABARAP. Researchers can employ western blotting to monitor LC3-II accumulation, immunofluorescence to assess colocalization of LC3 puncta with LAMP2-decorated lysosomes, and RT-qPCR profiling of autophagy-related genes. Cell viability assays under ER stress conditions??induced by tunicamycin or thapsigargin??can further define functional outcomes of CCPG1 loss. The CCPG1 Knockout MES-OV Polyclonal Cells serve as a versatile tool for advancing knowledge in autophagy, ovarian cancer biology, and drug resistance. For additional information, please contact Ascent Research.
